第19章集団の進化

A population's individuals often display different phenotypes, or express different alleles of a particular gene, which scientists refer to as polymorphisms. We call populations with two or more variations of particular characteristics polymorphic. A number of factors, including the population’s genetic structure and the environment (Figure 19.3) influence population variation, the distribution of phenotypes among individuals. Understanding phenotypic variation sources in a population is important for determining how a population will evolve in response to different evolutionary pressures.

Natural selection and some of the other evolutionary forces can only act on heritable traits, namely an organism’s genetic code. Because alleles are passed from parent to offspring, those that confer beneficial traits or behaviors may be selected, while deleterious alleles may not. Acquired traits, for the most part, are not heritable. For example, if an athlete works out in the gym every day, building up muscle strength, the athlete’s offspring will not necessarily grow up to be a body builder. If there is a genetic basis for the ability to run fast, on the other hand, a parent may pass this to a child.

Heritability is the fraction of phenotype variation that we can attribute to genetic differences, or genetic variability, among individuals in a population. The greater the heritability of a population’s phenotypic variation, the more susceptible it is to the evolutionary forces that act on heritable variation.

We call the diversity of alleles and genotypes within a population genetic variability. When scientists are involved in the breeding of a species, such as with animals in zoos and nature preserves, they try to increase a population’s genetic variability to preserve as much of the phenotypic diversity as possible. This also helps reduce associated risks of inbreeding, the mating of closely related individuals, which can have the undesirable effect of bringing together deleterious recessive mutations that can cause abnormalities and susceptibility to disease. For example, a disease that is caused by a rare, recessive allele might exist in a population, but it will only manifest itself when an individual carries two copies of the allele. Because the allele is rare in a normal, healthy population with unrestricted habitat, the chance that two carriers will mate is low, and even then, only 25 percent of their offspring will inherit the disease allele from both parents. While it is likely to happen at some point, it will not happen frequently enough for natural selection to be able to swiftly eliminate the allele from the population, and as a result, the allele maintains itself at low levels in the gene pool. However, if a family of carriers begins to interbreed with each other, this will dramatically increase the likelihood of two carriers mating and eventually producing diseased offspring, a phenomenon that scientists call inbreeding depression.

Changes in allele frequencies that we identify in a population can shed light on how it is evolving. In addition to natural selection, there are other evolutionary forces that could be in play: genetic drift, gene flow, mutation, nonrandom mating, and environmental variation.

The theory of natural selection stems from the observation that some individuals in a population are more likely to survive longer and have more offspring than others; thus, they will pass on more of their genes to the next generation. A big, powerful male gorilla, for example, is much more likely than a smaller, weaker one to become the population’s silverback, the pack’s leader who mates far more than the other males of the group. The pack leader will father more offspring, who share half of his genes, and are likely to also grow bigger and stronger like their father. Over time, the genes for bigger size will increase in frequency in the population, and the population will, as a result, grow larger on average. That is, this would occur if this particular selection pressure, or driving selective force, were the only one acting on the population. In other examples, better camouflage or a stronger resistance to drought might pose a selection pressure.

Another way a population’s allele and genotype frequencies can change is genetic drift (Figure 19.4), which is simply the effect of chance. By chance, some individuals will have more offspring than others—not due to an advantage conferred by some genetically-encoded trait, but just because one male happened to be in the right place at the right time (when the receptive female walked by) or because the other one happened to be in the wrong place at the wrong time (when a fox was hunting).

Small populations are more susceptible to the forces of genetic drift. Large populations, alternatively, are buffered against the effects of chance. If one individual of a population of 10 individuals happens to die at a young age before it leaves any offspring to the next generation, all of its genes—1/10 of the population’s gene pool—will be suddenly lost. In a population of 100, that’s only 1 percent of the overall gene pool; therefore, it is much less impactful on the population’s genetic structure.

Natural events, such as an earthquake disaster that kills—at random—a large portion of the population, can magnify genetic drift. Known as the bottleneck effect, it results in suddenly wiping out a large portion of the gene pool (Figure 19.5). At once, the survivors' genetic structure becomes the entire population's genetic structure, which may be very different from the pre-disaster population.

Another scenario in which populations might experience a strong influence of genetic drift is if some portion of the population leaves to start a new population in a new location or if a physical barrier divides a population. In this situation, those individuals are an unlikely representation of the entire population, which results in the founder effect. The founder effect occurs when the genetic structure changes to match that of the new population’s founding fathers and mothers. Researchers believe that the founder effect was a key factor in the genetic history of the Afrikaner population of Dutch settlers in South Africa, as evidenced by mutations that are common in Afrikaners but rare in most other populations. This is probably because a higher-than-normal proportion of the founding colonists carried these mutations. As a result, the population expresses unusually high incidences of Huntington’s disease (HD) and Fanconi anemia (FA), a genetic disorder known to cause blood marrow and congenital abnormalities—even cancer. A. J. Tipping et al., “Molecular and Genealogical Evidence for a Founder Effect in Fanconi Anemia Families of the Afrikaner Population of South Africa,” PNAS 98, no. 10 (2001): 5734-5739, doi: 10.1073/pnas.091402398.